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Vertical distribution of hydrometeors in the most intense convective clouds over the Indian region during the summer monsoon season (JJAS) is described for ten climatologically important areas. Tropical Rainfall Measuring Mission Precipitation Radar (TRMM PR) 3D radar reflectivity data is used in the present study for 10 years (2001–2010). The study constructs a convective cloud cell based on reflectivity thresholds, known as most intense convective cloud. The cloud cells are formed by taking the maximum reflectivity (Ze) at each altitude in the convective area with at least one radar pixel containing reflectivity of 40 dBZ or more. TRMM 2A23 data was used to eliminate the stratiform clouds from our analyses. The Vertical structure of convective clouds were studied over the east and west coast of India, and observation shows that the east coast consists of a higher frequency of convective clouds with high reflectivity values in average vertical profiles. It is observed that over the northeastern parts of the Indian subcontinent, ~30 % of convective cells extend beyond 15-km height whereas it is only ~4 % over the central Bay of Bengal. Over the Western Ghats, ~13 % of the cells have their tops below the freezing level, i.e. warm clouds do give heavy rain here. The regional differences in the vertical profile are high between the 5- and 12-km altitude. Most intense convective cells (MICCs) with a cloud top height more than 10 and 15 km show different characteristics, and the Western Ghats shows the most intense average vertical profile. Above 12 km, the western coast shows increased reflectivity value. Convective intensity is higher over the land-dominated areas for the cloud cells and decreases when we restrict the cloud cells to a certain altitude.

The immune system has a critical role in orchestrating tissue healing. As a result, regenerative strategies that control immune components have proved effective 1 , 2 . This is particularly relevant when immune dysregulation that results from conditions such as diabetes or advanced age impairs tissue healing following injury 2 , 3 . Nociceptive sensory neurons have a crucial role as immunoregulators and exert both protective and harmful effects depending on the context 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 – 12 . However, how neuro–immune interactions affect tissue repair and regeneration following acute injury is unclear. Here we show that ablation of the Na V 1.8 nociceptor impairs skin wound repair and muscle regeneration after acute tissue injury. Nociceptor endings grow into injured skin and muscle tissues and signal to immune cells through the neuropeptide calcitonin gene-related peptide (CGRP) during the healing process. CGRP acts via receptor activity-modifying protein 1 (RAMP1) on neutrophils, monocytes and macrophages to inhibit recruitment, accelerate death, enhance efferocytosis and polarize macrophages towards a pro-repair phenotype. The effects of CGRP on neutrophils and macrophages are mediated via thrombospondin-1 release and its subsequent autocrine and/or paracrine effects. In mice without nociceptors and diabetic mice with peripheral neuropathies, delivery of an engineered version of CGRP accelerated wound healing and promoted muscle regeneration. Harnessing neuro–immune interactions has potential to treat non-healing tissues in which dysregulated neuro–immune interactions impair tissue healing. Experiments in mouse models show that Na V 1.8 +  nociceptors innervate sites of injury and provide wound repair signals to immune cells by releasing calcitonin gene-related peptide (CGRP).

In the present scenario, immunization is of utmost importance as it keeps us safe and protects us from infectious agents. Despite the great success in the field of vaccinology, there is a need to not only develop safe and ideal vaccines to fight deadly infections but also improve the quality of existing vaccines in terms of partial or inconsistent protection. Generally, subunit vaccines are known to be safe in nature, but they are mostly found to be incapable of generating the optimum immune response. Hence, there is a great possibility of improving the potential of a vaccine in formulation with novel adjuvants, which can effectively impart superior immunity. The vaccine(s) in formulation with novel adjuvants may also be helpful in fighting pathogens of high antigenic diversity. However, due to the limitations of safety and toxicity, very few human-compatible adjuvants have been approved. In this review, we mainly focus on the need for new and improved vaccines; the definition of and the need for adjuvants; the characteristics and mechanisms of human-compatible adjuvants; the current status of vaccine adjuvants, mucosal vaccine adjuvants, and adjuvants in clinical development; and future directions.

Stability concerns of organic solar cell devices have led to the development of alternative hole transporting layers such as NiO which lead to superior device life times over conventional Poly(3,4-ethylenedioxythiophene) Polystyrene sulfonate (PEDOT:PSS) buffered solar cells. From the printability of such devices, it is imperative to be able to print NiO layers in the organic solar cell devices with normal architecture which has so far remained unreported. In this manuscript, we report on the successful ink-jet printing of very thin NiO thin films with controlled thickness and morphology and their integration in organic solar cell devices. The parameters that were found to strongly affect the formation of a thin yet continuous NiO film were substrate surface treatment, drop spacing, and substrate temperature during printing. The effect of these parameters was investigated through detailed morphological characterization using optical and atomic force microscopy and the results suggested that one can achieve a transmittance of ~89% for a ~18 nm thin NiO film with uniform structure and morphology, fabricated using a drop spacing of 50 μm and a heat treatment temperature of 400 °C. The devices fabricated with printed NiO hole transporting layers exhibit power conversion efficiencies comparable to the devices with spin coated NiO films.

This manuscript discusses the relationship between women, technology manifestation, and likely prospects in the developing world. Using India as a case study, the manuscript outlines how Artificial Intelligence (AI) and robotics affect women’s opportunities in developing countries. Women in developing countries, notably in South Asia, are perceived as doing domestic work and are underrepresented in high-level professions. They are disproportionately underemployed and face prejudice in the workplace. The purpose of this study is to determine if the introduction of AI would exacerbate the already precarious situation of women in the developing world or if it would serve as a liberating force. While studies on the impact of AI on women have been undertaken in developed countries, there has been less research in developing countries. This manuscript attempts to fill that need.

Human interleukin-33 (IL-33) is a 270 amino acid protein that belongs to the IL-1 cytokine family and plays an important role in various inflammatory disorders. Neutrophil proteases (Cathepsin G and Elastase) and mast cell proteases (tryptase and chymase) regulate the activity of IL-33 by processing full-length IL-33 into its mature form. There is little evidence on the role of these mature forms of IL-33 in retinal endothelial cell signaling and pathological retinal angiogenesis. Here, we cloned, expressed, and purified the various mature forms of human IL-33 and then evaluated the effects of IL-33 95-270 , IL-33 99-270 , IL-33 109-270 , and IL-33 112-270 on angiogenesis in human retinal microvascular endothelial cells (HRMVECs). We observed that IL-33 95-270 , IL-33 99-270 , IL-33 109-270 , and IL-33 112-270 significantly induced HRMVEC migration, tube formation and sprouting angiogenesis. However, only IL-33 99-270 could induce HRMVEC proliferation. We used a murine model of oxygen-induced retinopathy (OIR) to assess the role of these mature forms of IL-33 in pathological retinal neovascularization. Our 3′-mRNA sequencing and signaling studies indicated that IL-33 99-270 and IL-33 109-270 were more potent at inducing endothelial cell activation and angiogenesis than the other mature forms. We found that genetic deletion of IL-33 significantly reduced OIR-induced retinal neovascularization in the mouse retina and that intraperitoneal administration of mature forms of IL-33, mainly IL-33 99–270 and IL-33 109–270 , significantly restored ischemia-induced angiogenic sprouting and tuft formation in the hypoxic retinas of IL-33 –/– mice. Thus, our study results suggest that blockade or inhibition of IL-33 cleavage by neutrophil proteases could help mitigate pathological angiogenesis in proliferative retinopathies. Human IL-33 mature forms drive pathological retinal angiogenesis Interleukin-33 plays a role in many diseases and biological processes. This study investigates how various IL-33 mature forms affects blood vessel creation in the eye, especially in eye diseases. The researchers used genetic and drug-related methods to study the effects of IL-33 on blood vessel formation in the eye, focusing on how it regulates cellular signaling. The research used both in vitro and in vivo methods to understand IL-33’s role in abnormal blood vessel growth, specifically in oxygen-induced eye disease, a model for diseases like premature retinopathy and some aspects of diabetic retinopathy. The research concludes that IL-33, especially its enzyme-processed forms, plays a key role in the development of proliferative retinopathies by promoting abnormal blood vessel growth in the eye. This new understanding of IL-33’s function could lead to new treatments for proliferative retinopathies. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

In this paper, the study is supported by design, FEA simulation, and practical RF measurements on fabricated single-port-cavity-based acoustic resonator for gas sensing applications. In the FEA simulation, frequency domain analysis was performed to enhance the performance of the acoustic resonator. The structural and surface morphologies of the deposited ZnO as a piezoelectric layer have been studied using XRD and AFM. The XRD pattern of deposited bulk ZnO film indicates the perfect single crystalline nature of the film with dominant phase (002) at 2θ = 34.58°. The AFM micrograph indicates that deposited piezoelectric film has a very smooth surface and small grain size. In the fabrication process, use of bulk micro machined oxide (SiO2) for the production of a thin membrane as a support layer is adopted. A vector network analyzer (Model MS2028C, Anritsu) was used to measure the radio frequency response of the resonators from 1 GHz to 2.5 GHz. As a result, we have successfully fabricated an acoustic resonator operating at 1.84 GHz with a quality factor Q of 214 and an effective electromechanical coupling coefficient of 10.57%.

Brain metastasis (BrM) is a major problem associated with cancer-related mortality, and currently, no specific biomarkers are available in clinical settings for early detection. Liquid biopsy is widely accepted as a non-invasive method for diagnosing cancer and other diseases. We have reviewed the evidence that shows how the molecular alterations are involved in BrM, majorly from breast cancer (BC), lung cancer (LC), and melanoma, with an inception in how they can be employed for biomarker development. We discussed genetic and epigenetic changes that influence cancer cells to breach the blood-brain barrier (BBB) and help to establish metastatic lesions in the uniquely distinct brain microenvironment. Keeping abreast with the recent breakthroughs in the context of various biomolecules detections and identifications, the circulating tumor cells (CTC), cell-free nucleotides, non-coding RNAs, secretory proteins, and metabolites can be pursued in human body fluids such as blood, serum, cerebrospinal fluid (CSF), and urine to obtain potential candidates for biomarker development. The liquid biopsy-based biomarkers can overlay with current imaging techniques to amplify the signal viable for improving the early detection and treatments of occult BrM.

Cancer cells actively promote aerobic glycolysis to sustain their metabolic requirements through mechanisms not always clear. Here, we demonstrate that the gatekeeper of mitochondrial Ca 2+ uptake, Mitochondrial Calcium Uptake 1 (MICU1/CBARA1) drives aerobic glycolysis in ovarian cancer. We show that MICU1 is overexpressed in a panel of ovarian cancer cell lines and that MICU1 overexpression correlates with poor overall survival (OS). Silencing MICU1 in vitro increases oxygen consumption, decreases lactate production, inhibits clonal growth, migration and invasion of ovarian cancer cells, whereas silencing in vivo inhibits tumour growth, increases cisplatin efficacy and OS. Mechanistically, silencing MICU1 activates pyruvate dehydrogenase (PDH) by stimulating the PDPhosphatase-phosphoPDH-PDH axis. Forced-expression of MICU1 in normal cells phenocopies the metabolic aberrations of malignant cells. Consistent with the in vitro and in vivo findings we observe a significant correlation between MICU1 and pPDH (inactive form of PDH) expression with poor prognosis. Thus, MICU1 could serve as an important therapeutic target to normalize metabolic aberrations responsible for poor prognosis in ovarian cancer. The mitochondrial uniporter MICU1 regulates mitochondrial Ca 2+ uptake. Here, the authors show that MICU1 is upregulated in ovarian cancer and confers resistance to cisplatin-induced apoptosis through a Ca 2+ -mediated regulation of pyruvate dehydrogenase activity that results in increased glycolysis.